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Welcome to Our Parkinson's Place

I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's diseases as well and thought it would be nice to have a place where updated news is in one place. That is why I began this blog.

I am not responsible for it's contents, I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish. This is for you to read and to always keep an open mind.

Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please no advertisers. This is a free site for all.

Thank you.

Saturday, December 24, 2016

Learning you or a loved one has Parkinson’s disease can be devastating news. Parkinson’s can ultimately rob someone of their independence, their dignity and much more. It can also mean significant changes for a spouse or caregiver as they adjust to a new role.

Parkinson’s is a complex neurodegenerative disease that includes loss of dopamine in the brain. The exact causes are unknown, but likely involve a complex interaction between genetic and environmental factors. Symptoms include tremors, difficulty with movement and fine motor skills, depression and, ultimately, loss of balance and impaired cognition.

Approximately 13,300 British Columbians live with the disease, and this number will only increase as our population ages.

The good news is that Parkinson’s is one of the most treatable neurological conditions. Most people are able to control their symptoms for many years by working with physicians to find the right therapy. However, people with advanced Parkinson’s become frail and combinations of medications need to be delivered in the right dosage at the right time to maintain independence and quality of life. The difference between optimal versus ineffective therapy may be the difference between independent living and a hospital or nursing home.

In B.C. we are fortunate to have access to excellent programs and supports, including the University of B.C.-based Pacific Parkinson Research Centre, which is a Centre of Excellence for diagnosis and management of Parkinson’s. We also have excellent programs in Surrey, Kelowna and on Vancouver Island.

Key to effective treatment is early diagnosis. There is no single test for Parkinson’s, and many other conditions may mimic the disease, so a comprehensive exam by a neurologist with additional experience in Parkinson’s is required. Unfortunately, patients can face long waits of up to 24 months, which often means delayed treatment and unnecessary disease progression. Once diagnosed, patients often find health professionals such as nurses and physiotherapists lack knowledge of Parkinson’s and best practices. This means patients can receive improper treatment in emergency rooms, hospitals and care homes.

For all of these reasons, Parkinson Society British Columbia has developed a five-point plan to better co-ordinate and increase access to critical supports and services and deliver better care.

Parkinson’s already costs the B.C. health system about $112 million in annual direct costs and we believe we can help reduce future impacts by making strategic investments we estimate will cost less than $2 million a year. We forecast that admissions to hospitals and long-term care will be significantly reduced by developing a B.C. strategy — adding staff to existing Parkinson’s programs, funding specific training for allied health professionals, expanding the deep-brain stimulation program and funding levodopa/carbidopa intestinal gel for selected advanced Parkinson patients with no other options to maintain their independence.

Funding levodopa/carbidopa intestinal gel to a small number of advanced Parkinson patients is an example where strategic funding may be cost effective to the healthcare system as a whole. A short video on our website, tinyurl.com/ParkinsonGel, shows the incredible impact this therapy would have for the estimated 10 to 12 B.C. patients per year who would benefit.

By taking action in five areas, the province can help those with Parkinson’s lead independent lives for as long as possible and reduce their overall impact on the healthcare system.

Jean Blake is CEO of the Parkinson Society B.C.; Dr. Martin McKeown is UBC/PPRI chairman in Parkinson’s research, director of the Pacific Parkinson’s Research Centre and a medical advisor to Parkinson Society B.C.

Two techniques that detect prion protein oligomers in body fluids have made valuable improvements, say researchers. Each exploits the ability of certain toxic protein conformers to seed the misfolding and polymerization of the healthy, monomeric variety. Scientists led by Gianluigi Zanusso, University of Verona, Italy, report in the December 12 JAMA Neurology that real-time quaking-induced conversion (RT-QuIC) can now ferret out sporadic Creutzfeldt-Jakob disease (sCJD) prions in the CSF with near-perfect sensitivity and specificity. In the December 21 Science Translational Medicine, Claudio Soto of the University of Texas Medical School at Houston and colleagues report that they can use protein misfolding cyclic amplification (PMCA) to detect variant CJD (vCJD) in the blood. In a separate December 5 JAMA Neurology paper, Soto describes the potential application of the technology to detect α-synuclein in patients with Parkinson’s disease (PD). Scientists agree that these techniques will help better diagnose this group of devastating neurodegenerative disorders.

“These methods will have a major impact in the field,” wrote Inga Zerr, German Center for Neurodegenerative Diseases (DZNE), Göttingen, who was not involved in the studies. Jiri Safar of Case Western Reserve University in Cleveland agreed, saying the technology has widespread support amongst the small community of prion researchers. “It’s definitely a paradigm-changer, perhaps equivalent to the discovery of PCR amplification.” Safar directs the National Prion Disease Pathology Surveillance Center, where scientists monitor human cases of prion diseases for vCJD, the type that comes from eating beef contaminated with the prion that causes bovine spongiform encephalopathy (BSE).

Prion Hunters

Both PMCA and RT-QuIC hinge on the idea that protein monomers are slow to aggregate on their own, but if oligomers are present, fibrils come together quickly. PMCA was developed in Soto’s lab, but has been slow to catch on (Saborio et al., 2001). It mixes sample test fluid in a tube with normal protein monomers purified from healthy animal brain homogenates. If the sample contains no oligomers, the monomers stay monomers. In the presence of oligomers, monomers misfold, eventually incorporating into fibrils. After fibrils are allowed to grow for a while, mechanical forces break them into smaller oligomers, creating more seeds for another round of templated misfolding, and so on. This amplifies the oligomer signal so that the technique can detect as little as a single oligomer (Saá et al., 2006). Fibrils are then visualized by western blot with an anti-PrP antibody.

PMCA inspired RT-QuIC, which was developed by Byron Caughey at the National Institutes of Health in Bethesda, Maryland. The concept is similar, except the reaction takes place in a 96-well plate, the protein monomers are recombinant, and samples are shaken to hasten protein interactions and shorten incubation times. Amyloid fibrils are then detected by thioflavin T (ThT), a fluorescent dye, allowing the method to be completely automated. Since this technique is cheaper, easier, and faster than PMCA, it may be more widely adopted for routine lab use, said Safar. However, PMCA may complement RT-QuIC by detecting different types of prions and in the sorts of questions it can answer, he added.

RT-QuIC

Efforts are underway to optimize RT-QuIC technology even further. By shortening the recombinant protein and raising the reaction temperature, RT-QuIC has become faster and more accurate (Orrú et al., 2015). Zanusso and colleagues tested this new and improved assay retrospectively in CSF and olfactory mucosa samples from 23 people who were neurologically healthy, 81 people with non-prion neurological disorders, and 86 who were suspected sCJD patients. The Italian CJD surveillance system had initially diagnosed the last group with probable, possible, or suspected CJD. The patients were monitored until they either died or got another diagnosis. It turned out that 61 had a final diagnosis of sCJD, six a genetic form of CJD, and 17 a different neurological disease.

First authors Matilde Bongianni, Christina Orrú, and Bradley Groveman detected prions in the CSF and/or OM of all of the 61 confirmed sCJD patients, suggesting the RT-QuIC detection rate is 100 percent. None of the controls tested positive. The assay only detected prions in four of the six genetic CJD cases, suggesting the technique doesn’t work as well for prion strains that cause familial disease.

“The procedure should soon become the standard laboratory examination for the diagnosis of sporadic CJD,” wrote Paul Brown, formerly of the National Institutes of Health, in an accompanying editorial. “At last, we have a truly practical procedure for the diagnosis of sporadic CJD.” He added that it is still unclear whether it will detect prions in people who are asymptomatic.

RT-QuIC could be used to detect prions on hospital equipment or in transplanted tissue and organs, and monitor for the passage of prion diseases from animals to humans, said Safar. He and colleagues have run thousands of human CSF samples using RT-QuIC (Foutz et al., 2016). “It’s already changing our view of prion pathogenesis,” he said. Being able to detect minute quantities of prions has allowed researchers to detect the proteins in tissues where they hadn’t been seen before, he said.

A recent multicenter study validated RT-QuIC against neuropathologically confirmed cases of sporadic and genetic CJD (Cramm et al., 2016). It found that the assay had a sensitivity of 85 percent and a specificity of 99 percent. What’s more, it was almost perfectly reproducible between centers. Multiple labs are using it now, said Safar.

PMCA Struts Its Stuff in the Blood

Scientists are unsure why, but RT-QuIC poorly detects the vCJD strain of prion. In the United Kingdom, researchers estimate 30,000 people were exposed to this strain by eating BSE-tainted beef and could be asymptomatic carriers of the prion. Silent carriers are thought to have donated blood that caused infections in other people. A blood test for vCJD could prevent that. PMCA detects vCJD in blood from primates, and in human blood spiked with vCJD prions, but whether it detects the prion in samples from people who have CJD has been an open question (Jun 2014 news; Edgeworth et al., 2011).

Now, Soto and colleagues have used PMCA to test blood samples from 14 human vCJD patients. As control samples, first author Luis Concha-Marambio used blood from 153 people who were either cognitively healthy or had sCJD, or another neurodegenerative or neurological disorder. PMCA detected prion in all 14 samples with vCJD but in none of the controls. The test worked in only a few microliters of blood. Though double-blind studies with larger numbers of patients will be required before researchers can draw firm conclusions about sensitivity and specificity, this suggests PMCA can detect vCJD in symptomatic patients. “Detection of abnormal PrP in blood of variant CJD cases bears huge potential for early and potentially presymptomatic testing for individuals at risk,” wrote Zerr. Whether it will help screen donated blood remains to be seen.

Can PMCA Work for Non-Prions?

Soto has already used PMCA to detect Aβ oligomers in the CSF of AD patients (Mar 2014 news). Though this assay has not been widely used for that purpose, he is now examining whether it can pick up oligomers of α-synuclein in the CSF as well. If α-synuclein works as a biomarker in PD, it could aid in clinical and differential diagnosis, he said.

First author Mohammad Shahnawaz tested the CSF of 76 patients clinically diagnosed with PD. He also tested 10 patients each with dementia with Lewy bodies (DLB) and multiple system atrophy (MSA)—two other α-synuclein-related disorders. He compared those samples to CSF collected from 97 controls who had other neurologic or neurodegenerative diseases, including AD, or who were cognitively healthy. PMCA detected α-synuclein oligomers in 67 of the 76 PD patients, all of the DLB patients, and in eight people with MSA. Because clinical diagnosis of PD is not completely accurate, some of the cases may have been misdiagnosed, the authors suggested. Twelve controls tested positive as well. Shahnawaz and colleagues wrote that five were AD cases, which often have α-synuclein aggregates as a co-pathology, and two of the positive controls went on to develop PD a few years later, hinting that the test could detect oligomers before symptoms appear. Notwithstanding, an overall specificity of 96.0 percent and sensitivity of 88.5 percent suggests the test could be helpful in diagnosing disease.

“This provides proof of concept that the technology can be adapted to work in Parkinson’s disease, at a very high level of sensitivity and specificity,” Soto told Alzforum. Only further studies can say whether this test will be useful for monitoring progression or detecting prodromal disease, the authors wrote.

Henrik Zetterberg, University of Gothenburg, Sweden, found the results very interesting. “I would almost call them groundbreaking,” he told Alzforum. Since there are currently no reliable PD biomarkers, this stands a chance of becoming widely adopted, he suggested. However, he pointed out that the assay is technically challenging, with a long incubation time, which might limit its routine use. RT-QuIC, with its shorter lag time, might be better adapted for PD, he said. Researchers recently detected α-synuclein aggregates in the CSF of people using that assay, though they used only a small number of PD cases (Fairfoul et al., 2016).

“I’m excited to see many different labs using independent assays to confirm the potential use of α-synuclein oligomers as a marker for disease,” said Omar El-Agnaf, Hamad Bin Khalifa University, Doha, Qatar. He cautioned that the PMCA assay is not quantitative, and that the authors cannot rule out the possibility of cross-seeding from oligomers of other proteins, such as tau and Aβ, though they tested for this cross-seeding and did not observe it. He also noted that the reproducibility of the assay is questionable, so it may not be ideal for clinical use yet. “We have to work harder to find simpler, more sensitive, and specific assays that will help with diagnosis and prognosis,” said El-Agnaf.

Soto ultimately wants to use PMCA to test the blood of PD patients. He has founded a company, Amprion Inc., to commercialize the test.—Gwyneth Dickey Zakaib

(PHILADELPHIA, PA) -- Light of Day Philadelphia: Songwriters Up Close & Personal will take place on Saturday, January 7 at World Cafe Live. The event features performances by Eric Bazilian of the Hooters, Chuck Prophet, Willie Nile, Jeffrey Gaines, Ben Arnold, Joe D’Urso, Sharon Little, and Soraia. Showtime is 8:00pm. Tickets are $20 in advance; $25 at the door.

Proceeds go to raise money for the Light of Day Foundation, which utilizes the power of music to raise money and awareness in its continuing battle to defeat Parkinson’s disease and related neuro-degenerative diseases, specifically Progressive Supranuclear Palsy (PSP) and Amyotrophic Lateral Sclerosis (ALS), within our lifetime.

This show is one of many to take place over 10 days from January 6-16, 2017 follown holiday season tours of Europe and Canada. Shows will bring over 150 music acts to 30 venues in New Jersey, New York City, and Philadelphia.

62-year-old John Hook decided to donated the tree to Milord Lodge care home through the Parkinson’s UK charity because he has experienced family members suffer from Parkinson’s Disease and wants to help those who suffer from the illness.

He said “I wanted to be able to give something back to the charity that helped my family. Being able to donate a Christmas tree to a place such as Milford Lodge Care Home is a great way to mark my long service, and it will bring Christmas joy for many residents.”

The real Christmas tree and decorations was delivered to the care home by John where he was met by care home manager, Sue Jarvis.

The home was nominated to receive them by Parkinson’s UK regional branch as they have had previous members cared for there.

Sue commented: “We are delighted to receive this wonderful tree from B&Q and a special thanks to John for such a caring and considerate way of celebrating his personal achievement at B&Q.

“Our residents will love the chance to look out on the tree every day as we will be putting it in the main entrance to the home.”

A second tree donated by John was raffled off at the regional Parkinson’s UK Christmas lunch last Thursday.

Hal Boshier, chairperson for Parkinson’s UK’s North Hertfordshire and Stevenage branch, said: “It’s such a generous thing for John to do. Being able to offer a tree to an organisation that supports our members is wonderful and then also getting a tree to raffle off to help us raise vital funds to continue our local support which is vital for all of those families who are struggling with Parkinson’s Disease.”

WATCH: A B.C. family says the provincial government seems to be ignoring the latest studies about a drug used to treat people with advanced cases of Parkinson's. For more than a year they've been lobbying Victoria to cover the cost of that drug and say the government's decision not to fund the treatment is based on out-of-date research. Nadia Stewart reports

A B.C. family says the provincial government seems to be ignoring the latest studies about a drug used to treat people with advanced cases of Parkinson’s disease.

Paddi Woods was diagnosed with the disease in 2008. She says every day is worse than the one before.

“Hell, in a word. It’s like living in hell,” Wood said.

Over the last several years, Woods has been on a cocktail of pills and in and out of hospital.

“A couple of weeks ago, I had an experience where my whole chest had frozen. I was gasping for breath. It was terrifying. I was going in and out of consciousness,” she said.

Her daughter, Jenny, describes those episodes as “off periods” where her mom’s body freezes up.

“She cannot walk, she cannot stand, she cannot breathe,” Jenny said.

Those who have the disease don’t have enough dopamine in their body. According to Parkinson’s Society B.C., 13,000 people in the province live with the condition, but for about a dozen of them — including Woods — they lose their ability to control their body’s movements.

“Mom’s movements, her legs and her arms go crazy and she cannot sit still. She and my dad will dance around the kitchen to combat the dyskinesia,” Jenny said.

For Woods and those like her, pills just don’t work anymore. Her doctor says she needs Duodopa. Hooked up to an insulin-pump-type machine, the drug would deliver a steady dose of levodopa and carbidopa.

Health Canada has approved the drug, but B.C. won’t cover the cost of it. Jenny said she has written every MLA in B.C., along with the premier and prime minister, lobbying them to get the ministry of health to reconsider its position.

“If this pump does not come to B.C. for these people, for my mom, then in my opinion they have failed and I will be ashamed to be from this province,” Jenny said.

Duodopa’s cost, effectiveness cited as reasons for rejection

On Dec. 13, Eric Lun, executive director of B.C.’s Drug Intelligence and Optimization Branch, responded to Jenny Wood’s request for the province to reconsider its current position. Lun said Duodopa was examined by the Common Drug Review (CDR) in 2009. The recommendation then was for the drug to not be covered by participating PharmaCare programs. Among the two key reasons listed, one of them was the cost.

“At the manufacturer’s list price of $166/day, the annual cost of therapy with Duodopa is over $60,000 per patient per year, compared with $3 per day or approximately $1,095 for the oral forms of the same drug,” Lun wrote. “This represents a 5,379 per cent increase in the price of levodopa‑carbidopa from the oral form to the Duodopa form of the drug.”

Concerns were also raised about the quality of the two evaluated trials presented by the drug’s manufacturer, Abbvie. Citing the Canadian Expert Drug Advisory Committee, Lun said the trials were “open‑label, of small size, had high proportions of withdrawals, and were in patient populations that did not represent those most likely to use Duodopa.”

Jean Blake, executive director of Parkinson’s Society B.C., said the province should reconsider its position based on new research currently available.

“We do have evidence that it will make an incredible difference on these few people’s lives,” Blake said, referencing a 2014 article published in the Lancet Neurology medical journal. According to Blake, the evidence presented in this article was compelling enough to convince Ontario, Quebec and Alberta to approve coverage of the drug on a case-by-case basis.

In an email to Global News, the ministry of health said Abbvie is welcome to “forward a resubmission for Duodopa to the CDR for additional review. At this time, the manufacturer has indicated to the province that they have new data but are not willing to resubmit Duodopa to the CDR.”

Blake said the manufacturer is hesitant to resubmit, as it could impact coverage of the drug in other provinces.

“[Abbvie] has indicated they have done this new research and the benefits were of such a great magnitude, it was covered immediately in the U.S. We know it’s been covered in Europe for quite some time, as well,” Blake said. “The other five jurisdictions [in Canada] when the evidence was presented to them just said yes, it makes sense that this would be available to those few people who require it.”

However, Woods said this is about more than just compelling evidence.

“I want to know why the government thinks they have the right to make the decisions about whether we should live or die or whether we should have a life or not,” she said.

Friday, December 23, 2016

LIKE the best decisions in life, it was made at the top of Mount Kilimanjaro.

Bryn Williams, patent attorney and founder of Hillington-based Creation IP, decided to set up his own practice after scaling the biggest mountain in Africa.

While conquering a near 6,000-metre summit is likely to give perspective to the best of us, it had particular resonance for Mr Williams. By the time he made the gruelling climb in 2012, he had been living with Parkinson’s for five years, having been diagnosed with the neurological condition at just 36.

Reading through his blog from the time, the diagnosis was as devastating as one might imagine. With a wife, two young children and a good career, the life which had been mapped out before him took a sudden change of direction.

Yet, despite the dark times that inevitably followed, it paved the way for some genuinely life-affirming experiences. Driven by support from family and friends, Mr Williams responded to the shock by throwing himself into charity work, fulfilling a series of ambitions along the way.

By the time he had scaled Kilimanjaro, Mr Williams and the army of followers who had signed up to his Wobbly Williams Foundation had raised hundreds of thousands of pounds to fund research into neurological conditions. Marathons and 10ks were run, mountains were climbed, and all manner of quirky fund-raising events, including the Wobbly Williams ball, were held.

Mr Williamson achieved all this while holding down his job as a patent attorney in the Glasgow office of Marks & Clerk. However, by 2012 something had to give.

Mr Williams is quick to emphasise that Marks & Clerk had offered “fantastic” support in the period since his diagnosis, allowing him to reduce his hours to fit in the increasing demands of the charity work. Eventually, though, the balancing act became too difficult.

“In 2012, I went up Kilimanjaro at the very start of the year, [and] I expected the Parkinson’s to get worse because of the altitude and lots of other stuff,” Mr Williams said. “And it kind of got better. I realised it was because all the stress of work had left me. So I came down that mountain and decided to set up on my own.

“The plan was to set up Creation and spend a day or two doing patent attorney work, and the rest doing the charity work.”

Mr Williams found there were immediate benefits to running his own practice. Freed from the constraints of working for a big firm, he found he started to enjoy working as a patent attorney again. He also no longer experienced that “Sunday evening feeling”.

Mr Williams said he set out to build the sort of company where people are “happy to go to their work”, which began in earnest with the recruitment of European trademark attorney Catriona Good in May 2013. Ms Good was followed by office manager Karen McCartney in August that year.

“We started to build a firm where the motto is to make money and have fun, and that’s what we try and do,” he said. “It has grown to nine people now.”

The firm now has four attorney and five administrative staff, with plans to take on three to five further attorneys, depending on the breadth of subjects it decides to cover. The long-term objective is to grow to between 16 and 18 staff in total.

“That gives everybody sufficient cover to go away on holiday and not think about work,” Mr Williams noted. “We change everybody’s passwords when they go on holiday, so they can’t log in to their email. We are very big on that sort of thing.”

Clients of Creation include the Scottish company behind the Trtl, now the best-selling travel pillow on Amazon, and Spex, the offshore technology company based in Aberdeen.

Asked to define how Creation differs from others, Mr Williams replied that the firm tries to put itself in the client’s shoes. He eschews giving the “safe advice” which many IP firms offer but isn’t always what clients need.

Mr Williams said: “We also cover the whole life cycle of an idea. We get involved with our clients right at the start of our ideas, and help form them ideas.

“If you get the right intellectual property, then your company flies.”

With business growing so rapidly – Creation recently moved into bigger offices at the Hillington Innovation Park – it is no surprise to hear that Mr Williams is no longer as hands-on at his charity.

But it took the intervention of his friends to convince him to slow down.

He recalls being told by a friend at a beer festival in Prague that the charity had become too big for him to run. The advice did not go down well, initially it least. “I was raging!” Mr Williams said. “I got up, went for a walk, came back and said, tell me more. He had been the nominated person of all my pals to tell me that I had to give up the charity work. So I did.”

The decision paid off. Mr Williams hired Sharon Kane, the former fundraising manager at Down’s Syndrome Scotland, who has raised more than £1 million in her first year. Mr Williams and his band of willing volunteers had raised a hugely commendable £950,000 in seven years.

Mr Williams remains involved in the charity, which now goes under the Funding Neuro name, as the chairman of the board of trustees. He also remains a figurehead for its fundraising events, including an “Evening of Elegance” in Aberdeen, which last year featured an appearance by Emeli Sande.

“Funding Neuro is much more serious affair,” he said. “The trial we are funding at the minute, which is going to start fairly soon, is for kids with brain tumours.”

The trial is based on a pioneering method of delivering drugs directly into the brain, which has been developed at the University of Bristol. Mr Williams himself is participating in a similar trial to treat Parkinson’s, which involves him travelling to Bristol once every four weeks for treatment. The technique, which can be used to deliver proteins for Parkinson’s sufferers or chemotherapy for brain tumours, will not cure Mr Williams’ condition. But it has halted its progress quite dramatically. “I think I’m back where I was two or three years ago, when the trial started,” he said. “I should have deteriorated at a rate. Everybody who sees me who hasn’t seen me for a year or two goes ‘whoa’. I’m now nine years in.”

Mr Williams said he is unable to comment in too much detail about the trial because talks are taking place with a major pharmaceutical firm over the commercialisation of the delivery system and the drugs used.

Should the deal not come off, Mr Williams said one option for Funding Neuro would be to fund the extension of the trial for a further year. His own, one-year trial is due to come to a close at the end of the year. And while there are many different programmes researching ways to alleviate and cure Parkinson’s, Mr Williams has “put all my eggs in this basket” with this trial.

“What I want to do is answer the question, “does GDNF [glial cell-derived neurtrophic factor] work for Parkinson’s disease?” he said.

“I don’t want it to be left hanging in the air. It’s frightening how big a deal this could be for so many people.”

SAN ANTONIO - The University of Texas at San Antonio received a $5.2 million federal grant to use its best brains to study the brain.

The National Institute of Neurological Disorders and Stroke chose UTSA through a special long-term funding program called the Outstanding Investigator Award.

Dr. Charles Wilson said he’s excited about his daunting and overwhelming job. At his UTSA lab, he’s mapping the brain, how it reacts and searching for the keys to stop degenerative disorders like Parkinson’s and Huntington’s.

“We are trying to figure out where that pattern of activity comes from or causes it, and how we can disrupt it or block it in order to make better treatments for Parkinson's disease,” Wilson said.

The common treatment for this type of disease is deep brain stimulation. The $5.2 million grant will allow Wilson to dig deeper for eight more years.

“Deep brain stimulation is actually electrodes implanted into the brain that stimulates on a regular basis, like a heart pacemaker, only in the brain,” Wilson said.

The federal grant will allow researchers to focus on the region of the brain that involves voluntary motor skills.

“We can suggest improvements as to how deep brain stimulation can be made better. We have collaborators who are actually using those methods and trying them out, and we can create better and better deep brain stimulations. That's what we are trying to do,” Wilson.

Current patients will benefit, no doubt, but their children who inherit disease will too.

"She sells seashells by the seashore," he told his neurosurgeon, Dr. Vibhor Krishna, with a smile. "Rubber baby buggy bumpers."

He wasn't just showing off. He was letting the doctor know that his speech had improved since he underwent experimental surgery the day before, when Krishna created a tiny lesion in Nickelson's brain to treat his Parkinson's disease and the side effects of the medication he takes to manage it.

Krishna used no scalpel. There was no drilling, either. Instead, Krishna's tool was a computer mouse that helped him deliver more than 1,000 high-intensity, focused ultrasound waves into Nickelson's brain.

The 61-year-old editor from Colorado was the second patient to undergo the treatment at Ohio State as part of a clinical research trial. The facility is one of three U.S. hospitals conducting the research involving patients who experience dyskinesia, which causes the involuntary movement associated with Parkinson's, as a result of taking medication used to treat the disease.

Currently, the "gold standard" treatment for Parkinson's and similar conditions is deep-brain stimulation, in which electrodes are placed in the brain and controlled by a pacemaker-like device, Krishna said.

Placing the electrodes involves drilling into the skull — something many patients decline. The therapy being tested at Ohio State and other sites provides a noninvasive way to target the part of the brain that sends abnormal signals.

"It's a paradigm shift. It's something that patients wanted for a long time," said Krishna, an assistant professor in Ohio State's neurosurgery department.

"The first time I sat through a procedure, it was transformation. You could control a patient's tremor without opening the skull, give them symptom control that's able to make an impact on their quality of life."

For his procedure, Nickelson's head was shaved and fitted into a halo frame to hold it steady for an MRI. His scalp was submerged in water that helped conduct the waves and keep the head cool.

For more than three hours, he lay there as doctors and technicians viewed his brain, found their target and delivered a dozen 10- to 13-second rounds of ultrasound from a neighboring room. While each single ray does not cause damage to the brain, 1,024 rays converging in a pinpoint spot creates a lesion.

In Nickelson's case, the lesion measures 6-by-4-by-5 milliliters and primarily treated the left side of his body by keeping those abnormal signals from being sent.

The team stopped several times during the treatment to determine if Nickelson's symptoms were improving. Dr. Barbara Changizi, a neurologist, ran him through a battery of tests.

Among other things, he was asked to open and close his fingers, twist his arm and tap his foot.

She ranked the rigidity, tremor and slowness in his movements. Nickelson started with a score of 16, improving to 6 by the end of the treatments. Krishna expects he'll improve even more over the next week.

The procedure already has been approved by the U.S. Food and Drug Administration to treat essential tremor, which causes involuntary shaking. Researchers hope this study will bring FDA approval for the treatment of Parkinson's disease and medication side effects.

They eventually want to expand the technology to treat epilepsy, psychiatric disorders such as obsessive-compulsive disorder, brain tumors and neuropathic pain, Krishna said.

Dr. Ali Rezai, a neurosurgeon and director of the Neurological Institute at Ohio State, said that Wexner is the only Midwest hospital participating in the study. Ohio State, the University of Virginia and the University of Maryland plan to recruit a total of 20 patients.

"We're thrilled about it," he said. "This adds a whole new dimension in the way we can help people. We can perform brain surgery without ever cutting the skin."

Nickelson said his symptoms started about 14 years ago. When he isn't on his medication, he experiences a symptom called dystonia, which causes cramping and makes it difficult for him to move and articulate his thoughts.

"It feels like moving through the molasses," he said. "Your brain is telling your arms and legs to move, and you can't quite push through all this molasses."

When he takes too much medication, he experiences dyskinesia, which he describes as jerking, flopping, twitching or shaking.

To avoid too much or too little, Nickelson must carefully keep track of time, sometimes taking his medication as often as every two hours. He also has to make sure he isn't driving when a dose is about to wear off. Sometimes, it wears off at at the office, meaning he has to take work home with him.

He said he hopes this experimental treatment brings back a better home-work balance.

Despite some discomfort during the procedure, Nichelson said he likely will opt to go through it again to improve his right side. So far, he's noticed improvement in his speech and other dystonia symptoms.

Nickelson knew about deep-brain stimulation, but didn't want wires put in his brain or the hassle of maintaining the pacemaker-like device.

"I've been following the progress of focused ultrasound for several years," he said the night before his surgery. "I've just been waiting for the chance to try it out."

Summary: The effect music has on people may be genetically determined by dopamine functionality, a new study reports.

Source: Aarhus University.

In more details, results showed mood improvement after music exposure in GG subjects and mood deterioration after noise exposure in GT subjects. Moreover, the music as opposed to noise environment decreased the striatal activity of GT subjects as well as the prefrontal activity of GG subjects while processing emotional faces. NeuroscienceNews.com image is for illustrative purposes only.

Sounds, such as music and noise, are capable of reliably affecting individuals’ moods and emotions, possibly by regulating brain dopamine, a neurotransmitter strongly involved in emotional behavior and mood regulation.

However, the relationship of sound environments with mood and emotions is highly variable across individuals. A putative source of variability is genetic background.

In this regard, a new imaging genetics study directed by Professor Elvira Brattico from Aarhus University and conducted in two Italian hospitals in collaboration with the University of Helsinki (Finland) has provided the first evidence that the effects of music and noise on affective behavior and brain physiology are associated with genetically determined dopamine functionality.

In particular, this study, published in the journal Neuroscience, revealed that a functional variation in dopamine D2 receptor gene (DRD2 rs1076560) modulates the impact of music as opposed to noise on mood states and emotion-related prefrontal and striatal brain activity, evidencing a differential susceptibility for the affect-modulatory effects of music and noise on the GG and GT genotypes.

In more details, results showed mood improvement after music exposure in GG subjects and mood deterioration after noise exposure in GT subjects. Moreover, the music as opposed to noise environment decreased the striatal activity of GT subjects as well as the prefrontal activity of GG subjects while processing emotional faces.

These results are novel in identifying a biological source of variability in the impact of sound environments on emotional responses. The first author of the study, Tiziana Quarto, Ph.D. student at University of Helsinki under supervision of Prof. Brattico, further comments:

“Our approach allowed the observation of the link between genes and phenotypes via a true biological path that goes from functional genetic variations (for which the effects on molecular function is known) to brain physiology subtending behavior. The use of this approach is especially important when the investigated behavior is complex and very variable across subjects, because this means that many biological factors are involved.”

“This study represents the first use of the imaging genetics approach in the field of music and sounds in general. We are really excited about our results because they suggest that even a non-pharmacological intervention such as music, might regulate mood and emotional responses at both the behavioral and neuronal level,” says Professor Elvira Brattico.

“More importantly, these findings encourage the search for personalized music-based interventions for the treatment of brain disorders associated with aberrant dopaminergic neurotransmission as well as abnormal mood and emotion-related brain activity.”

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Source:Aarhus University Image Source: NeuroscienceNews.com image is in the public domain.

Interaction between DRD2 variation and sound environment on mood and emotion-related brain activity

Sounds, like music and noise, are capable of reliably affecting individuals’ mood and emotions. However, these effects are highly variable across individuals. A putative source of variability is genetic background. Here we explored the interaction between a functional polymorphism of the dopamine D2 receptor gene (DRD2 rs1076560, G > T, previously associated with the relative expression of D2S/L isoforms) and sound environment on mood and emotion-related brain activity. Thirty-eight healthy subjects were genotyped for DRD2 rs1076560 (G/G = 26; G/T = 12) and underwent functional magnetic resonance imaging (fMRI) during performance of an implicit emotion-processing task while listening to music or noise. Individual variation in mood induction was assessed before and after the task. Results showed mood improvement after music exposure in DRD2GG subjects and mood deterioration after noise exposure in GT subjects. Moreover, the music, as opposed to noise environment, decreased the striatal activity of GT subjects as well as the prefrontal activity of GG subjects while processing emotional faces. These findings suggest that genetic variability of dopamine receptors affects sound environment modulations of mood and emotion processing.

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I am a wife, mother and grandmother. I was diagnosed in 2004 by a Neurologist and a Neurologist- Movement
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have dystonia of the feet and calves as well. In 2004, I had a major stroke and
was paralyzed on my left side. It took a year of Physical Therapy to regain 99%
back.

I feel strongly about
spreading the word about Parkinson's Disease as we travel throughout parts of
the United States. My husband Larry, married on August 2, 1966 to my best
friend.been married for 50 plus years. In 1967 he joined the Marine Corps as an enlisted Marine , then became a warrant officer 4 Selective and retired as a Capt serving over 22 years. ( A Mustang). I am fortunate to have the support of my family and friends. I also have a maltese named Spencer who is my Service dog.God has
truly blessed me and I am thankful. Parkinson's Awareness is important to
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